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| 1 | Oxidative stress,insulin resistance,dyslipidemia and type 2 diabetes mellitus显示文摘Oxidative stress is increased in metabolic syndrome and type 2 diabetes mellitus(T2DM) and this appears to underlie the development of cardiovascular disease,T2 DM and diabetic complications.Increased oxidative stress appears to be a deleterious factor leading toinsulin resistance,dyslipidemia,β-cell dysfunction,impaired glucose tolerance and ultimately leading to T2 DM.Chronic oxidative stress,hyperglycemia and dyslipidemia are particularly dangerous for β-cells from lowest levels of antioxidant,have high oxidative energy requirements,decrease the gene expression of key β-cell genes and induce cell death.If β-cell functioning is impaired,it results in an under production of insulin,impairs glucose stimulated insulin secretion,fasting hyperglycemia and eventually the development of T2 DM. | Surapon Tangvarasittichai | 2015 | World Journal of Diabetes2015，6，3： | 95 |
| 2 | Gut microbiota imbalance and colorectal cancer显示文摘The gut microbiota acts as a real organ. The symbiotic interactions between resident micro-organisms and the digestive tract highly contribute to maintain the gut homeostasis. However, alterations to the microbiome caused by environmental changes(e.g., infection, diet and/or lifestyle) can disturb this symbiotic relationship and promote disease, such as inflammatory bowel diseases and cancer. Colorectal cancer is a complex association of tumoral cells, non-neoplastic cells and a large amount of micro-organisms, and the involvement of the microbiota in colorectal carcinogenesis is becoming increasingly clear. Indeed, many changes in the bacterial composition of the gut microbiota have been reported in colorectal cancer, suggesting a major role of dysbiosis in colorectal carcinogenesis. Some bacterial species have been identified and suspected to play a role in colorectal carcinogenesis, such as Streptococcus bovis, Helicobacter pylori, Bacteroides fragilis, Enterococcus faecalis, Clostridium septicum, Fusobacterium spp. and Escherichia coli. The potential pro-carcinogenic effects of these bacteria are now better understood. In this review, we discuss the possible links between the bacterial microbiota and colorectal carcinogenesis, focusing on dysbiosis and the potential pro-carcinogenic properties of bacteria, such as genotoxicity and other virulence factors, inflammation, host defenses modulation, bacterial derived metabolism, oxidative stress and anti-oxidative defenses modulation. We lastly describe how bacterial microbiota modifications could represent novel prognosis markers and/or targets for innovative therapeutic strategies. | Johan Gagnière Jennifer Raisch Julie Veziant Nicolas Barnich Richard Bonnet Emmanuel Buc Marie-Agnès Bringer Denis Pezet Mathilde Bonnet | 2016 | World Journal of Gastroenterology2016，22，2： | 76 |
| 3 | Oxidative stress as a crucial factor in liver diseases显示文摘Redox state constitutes an important background of numerous liver disorders. The redox state participates in the course of inflammatory, metabolic and proliferative liver diseases. Reactive oxygen species(ROS) are primarily produced in the mitochondria and in the endoplasmic reticulum of hepatocytes via the cytochrome P450 enzymes. Under the proper conditions, cells are equipped with special molecular strategies that control the level of oxidative stress and maintain a balance between oxidant and antioxidant particles. Oxidative stress represents an imbalance between oxidant and antioxidant agents. Hepatocytic proteins, lipids and DNA are among the cellular structures that are primarily affected by ROS and reactive nitrogen species. The process results in structural and functional abnormalities in the liver. Thus, the phenomenon of oxidative stress should be investigated for several reasons. First, it may explain the pathogenesis of various liver disorders. Moreover, monitoring oxidative markers among hepatocytes offers the potential to diagnose the degree of liver damage and ultimately to observe the response to pharmacological therapies. The present report focuses on the role of oxidative stress in selected liver diseases. | Halina Cichoz-Lach Agata Michalak | 2014 | World Journal of Gastroenterology2014，20，25： | 70 |
| 4 | Myocardial reperfusion injury and oxidative stress: Therapeutic opportunities显示文摘Acute myocardial infarction(AMI) is the leading cause of death worldwide. Its associated mortality, morbidity and complications have significantly decreased with the development of interventional cardiology and percutaneous coronary angioplasty(PCA) treatment, which quick-ly and effectively restore the blood flow to the area previously subjected to ischemia. Paradoxi-cally, the restoration of blood flow to the ischemic zone leads to a massive production of reactive oxygen species(ROS) which generate rapid and severe damage to biomolecules, generating a phenomenon called myocardial reperfusion injury(MRI). In the clinical setting, MRI is associated with multiple complications such as lethal reperfusion, no-reflow, myocardial stunning, and reperfusion arrhythmias. Despite significant advances in the understanding of the mechanisms accounting for the myocardial ischemia reperfusion injury, it remains an unsolved problem. Although promising results have been obtained in experimental studies(mainly in animal models), these benefits have not been translated into clinical settings. Thus, clinical trials have failed to find benefits from any therapy to prevent MRI. There is major evidence with respect to the contribution of oxidative stress to MRI in cardiovascular diseases. The lack- of consistency between basic studies and clinical trials is not solely based on the diversity inherent in epidemiology but is also a result of the methodological weak-nesses of some studies. It is quite possible that pharmacological issues, such as doses, active ingredients, bioavailability, routes of administration, co-therapies, startup time of the drug intervention,and its continuity may also have some responsibility for the lack- of consistency between different studies. Furthermore, the administration of high ascorbate doses prior to reperfusion appears to be a safe and rational therapy against the development of oxidative damage associated with myocardial reperfusion. In addition, the association with N-acetylcysteine(a glutathione donor) and deferoxamine(an iron chelator) could improve the antioxidant cardioprotection by ascorbate, mak-ing it even more effective in preventing myocardial reperfusion damage associated with PCA following AMI. | Jaime González-Montero Roberto Brito Abraham IJ Gajardo Ramón Rodrigo | 2018 | World Journal of Cardiology2018，10，9： | 56 |
| 5 | Stress changes on major faults caused by M_w7.9 Wenchuan earthquake,May 12,2008显示文摘On May 12,2008,a magnitude 7.9 earthquake ruptured the Longmenshan fault system in Sichuan Province,China,collapsing buildings and killing tens of thousands people.As predicted,aftershocks may last for at least one year,and moreover,large aftershocks are likely to occur.Therefore,it is critical to outline the areas with potential aftershocks before reconstruction and resettling people as to avoid future disasters.It is demonstrated that the redistribution of stress induced by an earthquake should trigger successive seismic activity.Based on static stress triggering theory,we calculated the coseismic stress changes on major faults induced by the Wenchuan earthquake,with elastic dislocation the-ory and the multilayered crustal model.We also discuss the stress distribution and its significance for future seismic activity under the impact of the Wenchuan earthquake.It is shown that coulomb failure stress(CFS) increases obviously on the Daofu-Kangding segment of the Xianshuihe Fault,the Maqu and Nanping segment of the Eastern Kunlun Fault,the Qingchuan Fault,southern segment of the Min-jiang Fault,Pengxian-Guanxian Fault,Jiangyou-Guangyuan Fault,and Jiangyou-Guanxian Fault.The increased stress raises the probability of earthquake occurrence on these faults.Since these areas are highly populated,earthquake monitoring and early disaster alarm system are needed.CFS increases with a magnitude of 0.03―0.06 MPa on the Qingchuan Fault,which is close to the northern end of the rapture of Wenchuan earthquake.The occurrence of some strong aftershocks,including three events with magnitude higher than 5.0,indicates that the seismic activities have been triggered by the main shock.Aftershocks seem to migrate northwards.Since the CFS change on the Lueyang-Mianxian Fault located on the NEE of the Qingchuan Fault is rather small(±0.01 MPa),the migration of aftershocks might be terminated in the area near Hanzhong City.The CFS change on the western Qinling Fault is around 10 Pa,and the impact of static triggering can be neglected.The increment of CFS on the Pengxian-Guanxian Fault and Beichuan-Yingxiu Fault southwest to the main rupture is 0.005―0.015 MPa,which would facilitate earthquake triggering in these areas.Very few aftershocks in these areas indicate that the accumulated stress has not been released sufficiently.High seismic risk is predicated in these areas due to coseismic CFS loading.The Wenchuan earthquake released the accumulated CFS on the Fubianhe Fault,the Huya Fault,the Ha'nan-Qingshanwan Fault,and the Diebu-Bailongjiang Fault.The decrement of CFS changes on the Longquanshan Fault east to Chengdu City is about 0.002 MPa.The seismic activity will be depressed by decrement of CFS on these faults. | SHAN Bin XIONG Xiong ZHENG Yong DIAO FaQi | 2009 | Science China Earth Sciences2009，52，5： | 47 |
| 6 | Role of endoplasmic reticulum stress in the pathogenesis of nonalcoholic fatty liver disease显示文摘Nonalcoholic fatty liver disease(NAFLD)has emerged as a common public health problem in recent decades.However,the underlying mechanisms leading to the development of NAFLD are not fully understood.The endoplasmic reticulum(ER)stress response has recently been proposed to play a crucial role in both the development of steatosis and progression to nonalcoholic steatohepatitis.ER stress is activated to regulate protein synthesis and restore homeostatic equilibrium when the cell is stressed due to the accumulation of unfolded or misfolded proteins.However,delayed or insufficient responses to ER stress may turn physiological mechanisms into pathological consequences,including fat accumulation,insulin resistance,inflammation,and apoptosis,all of which play important roles in the pathogenesis of NAFLD.Therefore,understanding the role of ER stress in the pathogenesis of NAFLD has become a topic of intense investigation.This review highlights the recent findings linking ER stress signaling pathways to the pathogenesis of NAFLD. | Xue-Qun Zhang Cheng-Fu Xu Chao-Hui Yu Wei-Xing Chen You-Ming Li | 2014 | World Journal of Gastroenterology2014，20，7： | 41 |
| 7 | Oxidative stress, cardiolipin and mitochondrial dysfunction in nonalcoholic fatty liver disease显示文摘Nonalcoholic fatty liver disease(NAFLD) is today considered the most common form of chronic liver disease, affecting a high proportion of the population worldwide. NAFLD encompasses a large spectrum of liver damage, ranging from simple steatosis to steatohepatitis, advanced fibrosis and cirrhosis. Obesity, hyperglycemia, type 2 diabetes and hypertriglyceridemia are the most important risk factors. The pathogenesis of NAFLD and its progression to fibrosis and chronic liver disease is still unknown. Accumulating evidence indicates that mitochondrial dysfunction plays a key role in the physiopathology of NAFLD, although the mechanisms underlying this dysfunction are still unclear. Oxidative stress is considered an important factor in producing lethal hepatocyte injury associated with NAFLD. Mitochondrial respiratory chain is the main subcellular source of reactive oxygen species(ROS), which may damage mitochondrial proteins, lipids and mitochondrial DNA. Cardiolipin, a phospholipid located at the level of the inner mitochondrial membrane, plays an important role in several reactions and processes involved in mitochondrial bioenergetics as well as in mitochondrial dependent steps of apoptosis. This phospholipid is particularly susceptible to ROS attack. Cardiolipin peroxidation has been associated with mitochondrial dysfunction in multiple tissues in several physiopathological conditions, including NAFLD. In this review, we focus on the potential roles played by oxidative stress and cardiolipin alterations in mitochondrial dysfunction associated with NAFLD. | Giuseppe Paradies Valeria Paradies Francesca M Ruggiero Giuseppe Petrosillo | 2014 | World Journal of Gastroenterology2014，20，39： | 50 |
| 8 | Impact chaos control and stress release——A key for development of ultra fine vibration milling显示文摘Through our previous experimental and analytical studies, it has been discovered that the key for the development of vibration milling is the impact chaos control and stress release. The necessities for the chaos control and stress release are: (i) to strictly eliminate the sub-harmonics; (ii) to control the super-harmonics to a lower level and (iii) to load the system compressively with relatively higher period, in order that the vibration energy can be absorbed by the particles effectively and sufficiently. A new vibration model for ultra fine milling is proposed, which has wide applications in preparing ultra fine particles. | WANG Shulin(Department of Power Engineering, University of Shanghai for Science and Technology, Shanghai 200093, China) | 2002 | Progress in Natural Science:Materials International2002，12，5： | 40 |
| 9 | Protective effects of nitric oxide on salt stress-induced oxidative damage to wheat (Triticum aestivum L.)leaves显示文摘The changes of chlorophyll and malondialde-hyde (MDA) contents, plasma membrane permeability confirmed that 0.1 and 1 mmol/L sodium nitroprusside (SNP), a donor of nitric oxide (NO) in vivo, could markedly alleviate the oxidative damage to wheat (Triticum aestivum L.) leaves induced by 150 and 300 mmol/L NaCl treatments, respectively. Further results proved that NO significantly enhanced the activities of superoxide dismutase (SOD) and catalase (CAT), both of which separately contributed to the delay of O2- and H2O2 accumulation in wheat leaves under saltstress. Meanwhile, the accumulation of proline was apparently accelerated. Therefore, these results suggested that NO could strongly protect wheat leaves from oxidative damage caused by salt stress. | Haihua Ruan Wenbiao Shen Maobing Ye Langlai Xu | 2002 | Chinese Science Bulletin2002，47，8： | 37 |
| 10 | Influence of tectonic stress on coalification:Stress degradation mechanism and stress polycondensation mechanism显示文摘The function of pressure for coalification is a long-term controversial issue, and the main cause is that the strata pressure and the tectonic stress were confused, which are two different actions of 'pres-sure' . The former benefits the physical coalification but retards the chemical coalification, whereas the latter may not only affect the physical structure of coal but also promote its chemical composition changes. In accordance with the organic molecule evolution of coal, there are two kinds of basic mechanisms of the influence of the tectonic stress on the chemical coalification: the tectonic stress degradation and the tectonic stress polycondensation. The stress degradation mechanism is a process of that, when the tectonic stress acted on the large molecule of coal in the form of mechanical force or kinetic energy, some chemical bonds of low decomposed energy, such as aliphatic side-chain and oxygenic functional groups, were broken up and then were degraded into free radicals of less mo-lecular weight, and finally escaped from coal in the form of liquid organic matter (hydrocarbon). The stress polycondensation is considered that, under the control of the anisotropic tectonic stress, the condensed aromatic nucleus trend to be parallel arranged and to be enhanced through rotating or displacing of aromatic rings, the basic structural unit of coal (BSU) increases by directional develop-ment and preferential stack. X-ray diffraction (XRD), Fourier transformation infrared microspectroscopy (FTIR), and rock pyrolysis analysis (Rock-eval) were employed to study the deformed coal series and the non-deformed coal series. The results showed that, compared with the non-deformed coal, the de-formed coal exhibits particular characteristics: weaker aliphatic absorbance peak and stronger aro-matic absorbance peak, lower pyrolysed hydrocarbon yield, and more increscent BSU. The concepts of stress degradation mechanism and stress polycondensation mechanism presented here would not deny the dominant function of the temperature in coalification, but emphasize the 'catalysis' of the tectonic stress in coalification. | CAO DaiYong LI XiaoMing ZHANG ShouRen | 2007 | Science China Earth Sciences2007，50，1： | 36 |
| 11 | A meta-analysis of oxidative stress markers in schizophrenia显示文摘Oxidative stress has been identified as a possible element in the neuropathological processes of schizophrenia(SCZ).Alteration of oxidative stress markers has been reported in SCZ studies,but with inconsistent results.To evaluate the risk of oxidative stress to schizophrenia,a meta-analysis was conducted,including five markers of oxidative stress [thiobarbituric reactive substances(TBARS),nitric oxide(NO),catalase(CAT),glutathione peroxidase(GP) and superoxide dismutase(SOD)] in SCZ patients versus healthy controls.This study showed that TBARS and NO significantly increased in SCZ,while SOD activity significantly decreased in the disorganized type of SCZ patients.No significant effect size was found for the activities of GP and CAT in SCZ patients(P>0.05).Egger’s regression test observed no significant publication bias across the oxidative stress markers,but found high heterogeneities in all the 5 markers.The subgroup analysis suggested that the ethnicity,sample size of patients and sample sources may contribute to the heterogeneity of the results for TBARS,NO and SOD.The result further demonstrated the involvement of oxidative stress in the pathophysiology of schizophrenia. | ZHANG Ming1,2,ZHAO ZhongMing3,HE Lin1,2,4 & WAN ChunLing1,2 1 Bio-X Center,Key Laboratory for the Genetics of Developmental and Neuropsychiatric Disorders(Ministry of Education),Shanghai Jiao Tong University,Shanghai 200030,China 2 Institutes for Nutritional Sciences,Shanghai Institute of Biological Sciences,Chinese Academy of Sciences,Shanghai 200031,China 3 Departments of Biomedical Informatics,Psychiatry,and Cancer Biology,Vanderbilt University Medical Center,Nashville,TN 37232,USA 4 Institutes of Biomedical Sciences,Fudan University,Shanghai 200032,China | 2010 | Science China(Life Sciences)2010，53，1： | 32 |
| 12 | Numerical simulation of mechanisms of deformation,failure and energy dissipation in porous rock media subjected to wave stresses显示文摘The pore characteristics,mineral compositions,physical and mechanical properties of the subarkose sandstones were acquired by means of CT scan,X-ray diffraction and physical tests.A few physical models possessing the same pore characteristics and matrix properties but different porosities compared to the natural sandstones were developed.The 3D finite element models of the rock media with varied porosities were established based on the CT image processing of the physical models and the MIMICS software platform.The failure processes of the porous rock media loaded by the split Hopkinson pressure bar(SHPB) were simulated by satisfying the elastic wave propagation theory.The dynamic responses,stress transition,deformation and failure mechanisms of the porous rock media subjected to the wave stresses were analyzed.It is shown that an explicit and quantitative analysis of the stress,strain and deformation and failure mechanisms of porous rocks under the wave stresses can be achieved by using the developed 3D finite element models.With applied wave stresses of certain amplitude and velocity,no evident pore deformation was observed for the rock media with a porosity less than 15%.The deformation is dominantly the combination of microplasticity(shear strain),cracking(tensile strain) of matrix and coalescence of the cracked regions around pores.Shear stresses lead to microplasticity,while tensile stresses result in cracking of the matrix.Cracking and coalescence of the matrix elements in the neighborhood of pores resulted from the high transverse tensile stress or tensile strain which exceeded the threshold values.The simulation results of stress wave propagation,deformation and failure mechanisms and energy dissipation in porous rock media were in good agreement with the physical tests.The present study provides a reference for analyzing the intrinsic mechanisms of the complex dynamic response,stress transit mode,deformation and failure mechanisms and the disaster mechanisms of rock media. | JU Yang1,2,WANG HuiJie1,YANG YongMing1,HU QinAng3 & PENG RuiDong1 1 State Key Laboratory of Coal Resources and Safe Mining,Beijing Key Laboratory of Fracture and Damage Mechanics of Rock and Concrete,China University of Mining and Technology,Beijing 100083,China 2 Department of Mechanical and Manufacturing Engineering,University of Calgary,Calgary,Alberta,T2N 1N4,Canada 3 School of Environment and Civil Engineering,College of Engineering,Oklahoma State University,Stillwater,OK 74078,USA | 2010 | Science China(Technological Sciences)2010，53，4： | 32 |
| 13 | Response of the accumulation of proline in the bodies of Populus euphratica to the change of groundwater level at the lower reaches of Tarim River显示文摘The content of proline in the plant bodies is closely related to the converse-succession-resistant capability of the plants. In this paper, the relationship between the proline accumulation in the bodies of Populus euphratica and the change of groundwater level is analyzed by taking Popu-lus euphratica, the main community-building species of the desert riparian forests along the Tarim River, as the research object. The research results show that the accumulation of proline in the bodies of Populus euphratica is closely related to the change of groundwater level gradient under drought stress, it increases with the drawdown of groundwater level and the increase of moisture stress degree; the accumulation of proline in the bodies of Populus euphratica has two ex-tremely high points at the groundwater depth ranges of 3.64—5.14 m and 9.46—10.16 m. Combining the field investiga-tion and the analysis of the plots, it is considered that the groundwater level of 3.5—4.5 m is rational for the growth of Populus euphratica. The stress groundwater depth for the normal growth and the critical one for the survival of Popu-lus euphratica are below 4.5 m and 9—10 m respectively at the lower reaches of the Tarim River. | Yaning Chen Yapeng Chen Weihong Li Hongfeng Zhang | 2003 | Chinese Science Bulletin2003，48，18： | 31 |
| 14 | 不同盐胁迫处理下番茄种子萌发期的耐盐性研究(英文)显示文摘[Objective] The aim of this study was to provide the theoretical basis for screening and utilizing salt-tolerant tomato varieties as well as for cultivating salt-resistance.[Method] Salinity tolerance of tomato during seed germination under simple salt sodium chloride and double salt calcium nitrate or sodium chloride stress were studied by Petri dish culturing.[Result] As the two kinds salt concentration increased,the germination regularity,the germination rate,the germination index and the growing vigor index of tomato seedlings decreased,but the germination losing rate increased.When salt concentration was from 0.2% to 0.4%,there was little difference among all indexes under two kinds of salt stress.However,when salt concentration was from 0.6% to 1.0%,the difference among all indexes under two kinds of salt stress was significant.[Conclusion] Salinity tolerance of tomato seeds under double salt calcium nitrate or sodium chloride stress was higher than that under simple salt sodium chloride stress. | 马洪英 郭锐 李洪安 张远芳 | 2008 | Agricultural Science & Technology2008，9，4： | 32 |
| 15 | DYNAMIC RECOVERY AND DYNAMIC RECRYSTALLIZATION OF 7005 ALUMINIUM ALLOY DURING HOT COMPRESSION显示文摘Dynamic recovery and dynamic recrystallizatin behaviors of AA7005 aluminium alloy (Al - Zn - Mg) during hot compression are investigated by isothermal compression testing.The interdependence of flow stress,stress, strain rate,true strain and deformation temperature for the alloy is analyzed by introduc- ing Zener-Hollomon parameter. A steady - state flow of the 7005 alloy is confirmed to be a thermal- ly activated process.which is governed by rate-controlling mechanisms of dislocations.A hyperbolic sine relationship can satisfactorily correlate temperature, strain rate with flow stress through an Arrhe- nius term that involves thermal activation parameters. The dynamic recovery mechanisms of the alloy are discussed.Cross- slip of jogged screw dislocations is the main dynamic recovery mechanism over the deformation temperatures and strain rates.Subgrains are highly developed in the originally elongat- ed grains.The size of the subgrain increases with decrease of the natural logarithm of Zener- Hol - lomon parameter.Local dynamic recrystallization is operative when the alloy is deformed at temperature of 500℃ and strain rate of 0. 001s - 1. | J. Shen S. S. Xie and J. H. tang (General Research Institute for Non - ferrous Metals,Beijing 100088, China) | 2000 | Acta Metallurgica Sinica(English Letters)2000，13，1： | 33 |
| 16 | Weaning stress and gastrointestinal barrier development:Implications for lifelong gut health in pigs显示文摘The gastrointestinal(GI) barrier serves a critical role in survival and overall health of animals and humans. Several layers of barrier defense mechanisms are provided by the epithelial, immune and enteric nervous systems. Together they act in concert to control normal gut functions(e.g., digestion,absorption, secretion, immunity, etc.) whereas at the same time provide a barrier from the hostile conditions in the luminal environment. Breakdown of these critical GI functions is a central pathophysiological mechanism in the most serious GI disorders in pigs. This review will focus on the development and functional properties of the GI barrier in pigs and how common early life production stressors, such as weaning, can alter immediate and long-term barrier function and disease susceptibility.Specific stress-related pathophysiological mechanisms responsible for driving GI barrier dysfunction induced by weaning and the implications to animal health and performance will be discussed. | Adam J.Moeser Calvin S.Pohl Mrigendra Rajput | 2017 | Animal Nutrition2017，，4： | 33 |
| 17 | Dietary resveratrol improves antioxidant status of sows and piglets and regulates antioxidant gene expression in placenta by Keap1-Nrf2 pathway and Sirt1显示文摘Background: Resveratrol, a plant phenol, affords protection against inflammation and oxidative stress. The objective of this study was to investigate the effects of dietary resveratrol supplementation during pregnancy and lactation on the antioxidant status of sows and piglets and on antioxidant gene expression and pathway in placenta.Methods: Forty sows were allotted to 2 dietary treatments 20 d after breeding. Sows were fed a control diet and a control diet with 300 mg/kg resveratrol. Oxidative stress biomarkers and antioxidant enzymes were measured in the placenta, milk, and plasma of sows and piglets. Antioxidant gene expression and protein expression of Kelch-like ECH-associated protein 1-Nuclear factor E2-related factor 2(Keap1-Nrf2), nuclear factor kappa B-p65(NFκB-p65) and sirtuin1(Sirt1) were quantified in the placenta.Results: Dietary resveratrol increased the litter and piglets weaning weights. Antioxidant status in the milk, placenta and plasma of sows and piglets was partially improved by dietary resveratrol. In placenta, Nrf2 protein expression was increased and Keap1 protein expression was decreased by dietary resveratrol. The m RNA expression of antioxidant genes including catalase(CAT), glutathione peroxidase 1(GPX1), GPX4, superoxide dismutase 1(SOD1)and heme oxygenase 1(HO1), and phase 2 detoxification genes, including glutamate-cysteine ligase modifier(GCLM), microsomal glutathione S-transferase 1(MGST1) and UDP glucuronosyltransferase family 1 member A1(UGT1 A1), was increased by dietary resveratrol. Dietary resveratrol also increased Sirt1 and phosphorylated NFκB-p65 protein expression in the placenta. We failed to observe any influences of dietary resveratrol on pro-inflammatory cytokine levels, including those of interleukin 1β(IL-1β), IL-6, IL-8 and tumor necrosis factor α(TNF-α). However, we observed that the m RNA expression of IL-8 in placenta was reduced by maternal resveratrol. In addition, dietary resveratrol showed interactive effects with day of lactation on activities of SOD and CAT and levels of malonaldehyde(MDA) and hydrogen peroxide(H2 O2) in milk.Conclusions: Dietary resveratrol supplementation during pregnancy and lactation improves the antioxidant status of sows and piglets, which is beneficial to the reproductive performance of sows. Dietary resveratrol regulates placental antioxidant gene expression by the Keap1-Nrf2 pathway and Sirt1 in placenta. | Qingwei Meng Tao Guo Gaoqiang Li Shishuai Sun Shiqi He Baojing Cheng Baoming Shi Anshan Shan | 2018 | Journal of Animal Science and Biotechnology2018，9，3： | 33 |
| 18 | Ginsenoside Rgl protects against ischemic/reperfusioninduced neuronal injury through miR-144/Nrf2/ARE pathway显示文摘Ginsenoside Rg1 (Rg1),a saponin extracted from Panax ginseng,has been well documented to be effective against ischemic/ reperfusion (I/R)neuronal injury.However,the underlying mechanisms remain obscure.In the present study,we investigated the roles of Nrf2 and miR-144 in the protective effects of Rgl against I/R-induced neuronal injury.In OGD/R-treated PC12 cells,Rgl (0.01-1 μmol/L)dose-dependently attenuated the cell injury accompanied by prolonging nuclear accumulation of Nrf2,enhancing the transcriptional activity of Nrf2,as well as promoting the expression of ARE-target genes.The activation of the Nrf2/ARE pathway by Rgl was independent of disassociation with Keapl,but resulted from post-translational regulations.Knockdown of Nrf2 abolished all the protective changes of Rgl in OG-D/R-treated PC12 cells.Furthermore,Rgl treatment significantly decreased the expression of miR-144,which downregulated Nrf2 production by targeting its 3'-untranlated region after OGD/R.Knockdown of Nrf2 had no effect on the expression of miR-144,suggesting that miR-144 was an upstream regulator of Nrf2.We revealed that there was a direct binding between Nrf2 and miR-144 in PC12 cells.Application of anti-miR-144 occluded the activation of the Nrf2/ ARE pathway by Rgl in OGD/R-treated PC12 cells.In tMCAO rats,administration of Rgl (20 mg/kg).significantly alleviated ischemic injury,and activated Nff2/ARE pathway.The protective effects of Rgl were abolished by injecting of AAV-HIF-miR-144-shRNA into the predicted ischemic penumbra.In conclusion,our results demonstrate that Rgl alleviates oxidative,stress after I/R through inhibiting miR-144 activity and subsequently promoting the Nrf2/ARE pathway at the post-translational-level. | Shi-feng Chu Zhao Zhang Xin Zhou Wen-bin He Chen Chen Piao Luo Dan-dan Liu Qi-di Ai Hai-fan Gong Zhen-zhen Wang Hong-shuo Sun Zhong-ping Feng Nai-hong Chen | 2019 | Acta Pharmacologica Sinica2019，40，1： | 30 |
| 19 | From fatty liver to fibrosis:A tale of “second hit”显示文摘Although much is known about how fat accumulates in the liver,much remains unknown about how this causes sustained hepatocellular injury.The consequences of injury are recognized as nonalcoholic steatohepatitis(NASH) and progressive fibrosis.The accumulation of fat within the hepatocytes sensitizes the liver to injury from a variety of causes and the regenerative capacity of a fatty liver is impaired.An additional stressor is sometimes referred to as a 'second hit' in a paradigm that identifies the accumulation of fat as the 'first hit'.Possible candidates for the second hit include increased oxidative stress,lipid peroxidation and release of toxic products such as malondialdehyde and 4-hydroxynonenal,decreased antioxidants,adipocytokines,transforming growth factor(TGF)-β,Fas ligand,mitochondrial dysfunction,fatty acid oxidation by CYPs(CYP 2E1,4A10 and 4A14),and peroxisomes,excess iron,small intestinal bacterial overgrowth,and the generation of gut-derived toxins such as lipopolysaccharide and ethanol.Oxidative stress is one of the most popular proposed mechanisms of hepatocellular injury.Previous studies have specifically observed increased plasma and tissue levels of oxidative stress markers and lipid peroxidation products,with reduced hepatic and plasma levels of antioxidants.There is also some indirect evidence of the benefit of antioxidants such as vitamin E,S-adenosylmethionine,betaine,phlebotomy to remove iron,and N-acetylcysteine in NASH.However,a causal relationship or a pathogenic link between NASH and oxidative stress has not been established so far.A number of sources of increased reactive oxygen species production have been established in NASH that include proinflammatory cytokines such as tumor necrosis factor(TNF)-α,iron overload,overburdened and dysfunctional mitochondria,CYPs,and peroxisomes.Briefly,the pathogenesis of NASH is multifactorial and excess intracellular fatty acids,oxidant stress,ATP depletion,and mitochondrial dysfunction are important causes of hepatocellular injury in the steatotic liver. | Metin Basaranoglu Gkcen Basaranoglu Hakan Sentürk | 2013 | World Journal of Gastroenterology2013，19，8： | 28 |
| 20 | FoxO3a and disease progression显示文摘The Forkhead box O(FoxO) family has recently been highlighted as an important transcriptional regulator of crucial proteins associated with the many diverse functions of cells. So far, FoxO1, FoxO3 a, FoxO4 and FoxO6 proteins have been identified in humans. Although each FoxO family member has its own role, unlike the other FoxO families, FoxO3 a has been extensively studied because of its rather unique and pivotal regulation of cell proliferation, apoptosis, metabolism, stress management and longevity. FoxO3 a alteration is closely linked to the progression of several types of cancers, fibrosis and other types of diseases. In this review, we will examine the function of FoxO3 a in disease progression and also explore FoxO3a's regulatory mechanisms. We will also discuss FoxO3 a as a potential target for the treatment of several types of disease. | Richard Seonghun Nho Polla Hergert | 2014 | World Journal of Biological Chemistry2014，5，3： | 28 |
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